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We read with interest the study by Vikman et al. (1) and are pleased that this respectable group shares our interest in atrially induced heart rate turbulence. Although we understand the reasoning behind the suggestion that “vagal inhibition in response to premature atrial excitation is absent, or even that transient enhancement of vagal outflow occurs before atrial fibrillation,” we would like to offer the investigators an alternative explanation for their findings.

We all would surely agree that less effective ventricular contraction and compensatory pause after premature beats is responsible for transient hemodynamic deficit, missed baroreflex afferent input, and early vagal inhibition. This mechanism is applicable for both ventricular and atrial premature complexes (APCs). Autonomic modulation of sinus nodal discharge after APCs may explain values of turbulence onset (TO) ≤0. When TO >0 is found, the underlying mechanism has to be different. The mechanism suggested by Vikman et al., namely the temporary direct suppression of sinus node automaticity, is certainly plausible. This phenomenon, which may mask (or overwhelm) the autonomic component of early acceleration, has been previously demonstrated (2).

Because of a missing relationship between TO and APC prematurity, Vikman et al. rejected the hypothesis that sinus resetting is the predominant factor influencing the temporal changes of TO. However, this lack of correlation seems to us compatible rather than incompatible with sinus nodal resetting. Autonomically mediated TO should be positively related to the APC coupling interval, whereas TO mediated by direct suppression of sinus node automaticity should be negatively related to the APC coupling interval. Thus, coexistence of both mechanisms may effectively offset the relationship between TO and APC prematurity.

Although TO and turbulence slope after ventricular premature complexes and turbulence slope after APCs reflect heart rate vagal modulation, this is not the case for TO after APCs (3). We have not found any significant relationship between atrial TO and other previously established surrogates of heart rate vagal modulation in large Holter databases (Wichterle et al., unpublished data, 2005).

We thus wonder whether Vikman et al. (1) would agree that their finding might be interpreted as either 1) temporal decrease of vagal modulation, or 2) temporal change of APC prematurity (which cannot be exactly assessed from Holter recording) and/or site of origin of APCs—all factors potentially facilitating sinus node resetting. We believe that the latter possibility might be more probable because none of the other investigated indices of autonomic modulation (including spectral measures of heart rate variability and turbulence slope after APCs) revealed any significant change before the onset of spontaneous atrial fibrillation episode.

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